The onset and maintenance of AF is highly complex and the most frequent pathoanatomic changes in AF are atrial fibrosis. In recent years, experimental and clinical studies have demonstrated that atrial remodelling and dilation in AF depending on cellular hypertrophy, fibroblast proliferation and tissue fibrosis. Atrial fibrosis leads to disruption of the electrical side-to-side junctions between muscle bundles and has potentially arrhythmogenic mechanisms. The association of atrial fibrosis and AF has been the subject of intense recent investigation, and it is now widely accepted that interstitial fibrosis creates a substrate for arrhythmia. It is believed that when atrial myocardial fibre bundles are separated by connective tissue, the conduction properties are altered because of the effects on axial resistance, leading to arrhythmia. Myocardial fibrosis is preceded by a growing activity of extracellular matrix (ECM), pro-inflammatory cytokines and at the same time more pronounced collagen (type I and III) expression. Histological studies in patients with both AF and sick sinus syndrome have shown extensive fibrosis of the atrial muscle in the sinus node and internodal tracts. These results suggest that myocardial interstitial fibrosis plays a crucial role in AF .